Keynote Talk: The Intersection of Diet, Brain, Gut Microbiome and Behaviour - Intervening to Improve Cognition

Our research attempts to model the western lifestyle, investigating how provision of varied, energy rich diets can override the control mechanisms that should maintain body weight. Rats fed an obesogenic, cafeteria style diet consistently show deficits in hippocampal-dependent memory tasks, and reduced diversity of their gut microbiome compared to control rats. Such behavioural deficits were independent of weight differences, as rats consuming diets high in saturated fat or high in sugar, for just two weeks, had impaired spatial memory even in the absence of caloric excess. We found that the memory deficits were associated with changes in the gut microbiota composition and genes related to inflammation in the hippocampus, a key brain region for memory and learning.

More recently we have investigated whether the bacteriostatic antibiotic, minocycline, which is reported to exert anti-inflammatory effects, can modulate spatial memory. Again, cafeteria diet produced persistent deficits in spatial memory (novel place recognition) that were prevented by minocycline cotreatment. Of interest, chow fed rats treated with minocycline performed worse than those treated with vehicle. Faecal microbiota alpha diversity was reduced by both cafeteria diet and minocycline treatment, but these reductions were not associated with performance on the novel place task. However, abundances of specific OTUs within Bacteroides and Lactobacillus were associated with place task performance. Together, studies such as these suggest the gut microbiota could play a causal role in regulating behaviour. Current experiments are exploring the impact of fecal transfer on memory performance in rats consuming the obesogenic diet.